Receptors, Adrenergic, beta-2
A subclass of beta-adrenergic receptors (RECEPTORS, ADRENERGIC, BETA). The adrenergic beta-2 receptors are more sensitive to EPINEPHRINE than to NOREPINEPHRINE and have a high affinity for the agonist TERBUTALINE. They are widespread, with clinically important roles in SKELETAL MUSCLE; LIVER; and vascular, bronchial, gastrointestinal, and genitourinary SMOOTH MUSCLE.
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A group of polycyclic compounds closely related biochemically to TERPENES. They include cholesterol, numerous hormones, precursors of certain vitamins, bile acids, alcohols (STEROLS), and certain natural drugs and poisons. Steroids have a common nucleus, a fused, reduced 17-carbon atom ring system, cyclopentanoperhydrophenanthrene. Most steroids also have two methyl groups and an aliphatic side-chain attached to the nucleus. (From Hawley's Condensed Chemical Dictionary, 11th ed)
A generic expression for any tachycardia that originates above the BUNDLE OF HIS.
Abnormal cardiac rhythm that is characterized by rapid, uncoordinated firing of electrical impulses in the upper chambers of the heart (HEART ATRIA). In such case, blood cannot be effectively pumped into the lower chambers of the heart (HEART VENTRICLES). It is caused by abnormal impulse generation.
Abnormally rapid heartbeat, usually with a HEART RATE above 100 beats per minute for adults. Tachycardia accompanied by disturbance in the cardiac depolarization (cardiac arrhythmia) is called tachyarrhythmia.
Removal of tissue with electrical current delivered via electrodes positioned at the distal end of a catheter. Energy sources are commonly direct current (DC-shock) or alternating current at radiofrequencies (usually 750 kHz). The technique is used most often to ablate the AV junction and/or accessory pathways in order to interrupt AV conduction and produce AV block in the treatment of various tachyarrhythmias.
A phenethylamine found in EPHEDRA SINICA. PSEUDOEPHEDRINE is an isomer. It is an alpha- and beta-adrenergic agonist that may also enhance release of norepinephrine. It has been used for asthma, heart failure, rhinitis, and urinary incontinence, and for its central nervous system stimulatory effects in the treatment of narcolepsy and depression. It has become less extensively used with the advent of more selective agonists.
A collection of heterogenous conditions resulting from defective LIPID METABOLISM and characterized by ADIPOSE TISSUE atrophy. Often there is redistribution of body fat resulting in peripheral fat wasting and central adiposity. They include generalized, localized, congenital, and acquired lipodystrophy.
Lipodystrophy, Congenital Generalized
HIV-Associated Lipodystrophy Syndrome
Lipodystrophy, Familial Partial
Inherited conditions characterized by the partial loss of ADIPOSE TISSUE, either confined to the extremities with normal or increased fat deposits on the face, neck and trunk (type 1), or confined to the loss of SUBCUTANEOUS FAT from the limbs and trunk (type 2). Type 3 is associated with mutation in the gene encoding PEROXISOME PROLIFERATOR-ACTIVATED RECEPTOR GAMMA.
Lung Diseases, Obstructive
Any disorder marked by obstruction of conducting airways of the lung. AIRWAY OBSTRUCTION may be acute, chronic, intermittent, or persistent.
beta2-adrenergic receptor-selective agonist clenbuterol prevents Fas-induced liver apoptosis and death in mice. (1/192)Stimulation of the cAMP-signaling pathway modulates apoptosis in several cell types and inhibits Jo2-mediated apoptosis in cultured rat hepatocytes. No information is yet available as to whether the hepatic beta2-adrenergic receptor (AR) expression level, including beta2-AR-dependent adenylyl cyclase activation, modulates hepatocyte sensitivity to apoptosis in vivo or whether this sensitivity can be modified by beta2-AR ligands. We have examined this using C57BL/6 mice, in which hepatic beta2-AR densities are low, and transgenic F28 mice, which overexpress beta2-ARs and have elevated basal liver adenylyl cyclase activity. The F28 mice were resistant to Jo2-induced liver apoptosis and death. The beta-AR antagonist propranolol sensitized the F28 livers to Jo2. In normal mice clenbuterol, a beta2-AR-specific agonist, considerably reduced Jo2-induced liver apoptosis and death; salbutamol, another beta2-AR-selective agonist, also reduced Jo2-induced apoptosis and retarded death but with less efficacy than clenbuterol; and propranolol blocked the protective effect of clenbuterol. This indicates that the expression level of functional beta2-ARs modulates Fas-regulated liver apoptosis and that this apoptosis can be inhibited in vivo by giving beta2-AR agonists. This may well form the basis for a new therapeutic approach to diseases involving abnormal apoptosis. (+info)
Study of interaction between agonists and asn293 in helix VI of human beta(2)-adrenergic receptor. (2/192)Previously, we demonstrated the involvement of Asn293 in helix VI of the human beta(2)-adrenergic receptor in stereoselective agonist recognition and activation. In the present study, we have further explored the role of this residue by synthesizing derivatives of isoproterenol and clenbuterol, two beta-adrenergic receptor agonists. We analyzed their efficacy and affinity on the wild-type and a mutant receptor (Asn293Leu). Each compound had similar efficacy (tau values) on both the wild-type and mutant receptor, although tau values varied considerably among the eight compounds studied. It appeared that one derivative of isoproterenol, but not of clenbuterol, showed a gain in affinity from the wild type to the mutant receptor. This derivative had a methyl substituent instead of the usual beta-OH group in the aliphatic side chain of isoproterenol, compatible with the more lipophilic nature of the leucine side chain. Such a "gain of function" approach through a combination of synthetic chemistry with molecular biology, may be useful to enhance our insight into the precise atomic events that govern ligand-receptor interactions. (+info)
Rapid extraction of clenbuterol from human and calf urine using empore C8 extraction disks. (3/192)In the present paper, disk extraction was evaluated for the rapid isolation of clenbuterol from human and calf urine, followed by high-performance liquid chromatography analysis with UV detection. A method was developed for the extraction with standard density C8 disks. The disks could be washed with 25% methanol in 0.01M sodium hydroxide without significant losses of clenbuterol. The recovery of denbuterol was about 85%, and the extracts were clean. The detection limit was about 10 ng/mL. The main advantages of these disks were the saving of time and the reduced amounts of organic solvents needed. (+info)
Deleterious effects of chronic clenbuterol treatment on endurance and sprint exercise performance in rats. (4/192)The beta(2)-adrenergic agonist, clenbuterol, has powerful muscle anabolic and lipolytic effects and is used by athletes to improve exercise performance; however, its use in conjunction with different forms of exercise training has received limited attention. Since previous studies have reported that chronic use of other beta(2)-adrenergic agonists has deleterious effects on cardiac muscle structure and function, the aim of the present study was to determine whether chronic clenbuterol administration would reduce the exercise capabilities of rats subjected to long-term treadmill sprint running, endurance swimming or voluntary wheel running training. The effect of clenbuterol treatment on exercise performance in rats was evaluated in three separate studies. Different groups of male rats were assigned to an endurance swimming (2 h/day, 5/7 days, 18 weeks) group, a treadmill sprint running (8x1 min bouts, 1.05 m/s, 20 weeks) group, or a voluntary wheel running (16 weeks) group. In each study, rats were allocated into either a treated group that received clenbuterol (2 mg.kg(-1).day(-1)) in their drinking water or an untreated control group. In each of the three studies, treated rats exhibited a reduction in exercise performance compared with untreated rats. Treated rats ran approximately 57% less total distance than untreated rats in the voluntary running programme and were unable to complete the swimming and sprinting protocols performed by the untreated rats. In each of the studies, the treated rats exhibited cardiac hypertrophy, with absolute heart mass increased by approximately 19% and heart mass relative to body mass increased by approximately 20%. The hearts of sedentary rats treated with clenbuterol exhibited extensive collagen infiltration surrounding blood vessels and in the wall of the left ventricle. The results indicate strongly that chronic clenbuterol administration deleteriously affects exercise performance in rats, potentially due to alterations in cardiac muscle structure and function. (+info)
Effects of beta(2)-agonist clenbuterol on biochemical and contractile properties of unloaded soleus fibers of rat. (5/192)The effects of clenbuterol beta(2)-agonist administration were investigated in normal and atrophied [15-day hindlimb-unloaded (HU)] rat soleus muscles. We showed that clenbuterol had a specific effect on muscle tissue, since it reduces soleus atrophy induced by HU. The study of Ca(2+) activation properties of single skinned fibers revealed that clenbuterol partly prevented the decrease in maximal tension after HU, with a preferential effect on fast-twitch fibers. Clenbuterol improved the Ca(2+) sensitivity in slow- and fast-twitch fibers by shifting the tension-pCa relationship toward lower Ca(2+) concentrations, but this effect was more marked after HU than in normal conditions. Whole muscle electrophoresis indicated slow-to-fast transitions of the myosin heavy chain isoforms for unloaded and for clenbuterol-treated soleus. The coupling of the two latter conditions did not, however, increase these phenotypical transformations. Our findings indicated that clenbuterol had an anabolic action and a beta(2)-adrenergic effect on muscle fibers and appeared to counteract some effects of unloading disuse conditions. (+info)
Differential effects of dexamethasone and clenbuterol on rat growth and on beta2-adrenoceptors in lung and skeletal muscle. (6/192)Beta-adrenergic agonists increase growth rate, but their efficacy is reduced over time as the number of beta2-adrenoceptors in muscle decreases. Dexamethasone increases beta2-adrenoceptor density in many tissues, but this effect has not been reported in skeletal muscle. In this study, male rats were treated daily for 10 d with either clenbuterol (4 mg/kg of feed), dexamethasone (.2 mg/kg BW, s.c.), or clenbuterol plus dexamethasone. Untreated rats served as controls. Dexamethasone caused a marked suppression of growth rate, which resulted in decreased (P < .001) body weight (-29%), carcass weight (-30%), hind-limb muscles (-22%), omental fat (-22%), and heart weight (-10%). Feed intake was reduced (-26%), but feed conversion efficiency was also impaired (P < .001). Clenbuterol caused a small increase in growth rate (+6%; P < .05), with an increase in leg muscle (+7%; P < .01) and heart mass (+8%; P < .05). Feed efficiency was improved (P < .001) by clenbuterol. Rats given the combined treatment still showed a reduction in growth rate (-81%). Clenbuterol caused only a mild attenuation of the effects of dexamethasone on feed intake, BW, and carcass weight, but reduced the catabolic effect of dexamethasone on hind-limb muscle to only -8%. Clenbuterol caused a slight increase in the affinity beta2-adrenoceptors in lung for binding to the radioligand (-)[125I]iodocyanopindolol. Relative to control values, the density of beta2-adrenoceptors in lung was +31% with dexamethasone treatment, -45% with clenbuterol, and -23% with the combined treatment. Clenbuterol also decreased beta2-adrenoceptors in skeletal muscle (-35%), but so did dexamethasone (-13%), so the effects of the beta-adrenergic agonist were not attenuated through use of the combined treatment (-40%). The results show that the inductive effect of glucocorticoids on beta2-adrenoceptors is tissue-specific and that glucocorticoid treatment is not a useful adjunct to beta-adrenergic agonist treatment in animal production. (+info)
Power output of fast and slow skeletal muscles of mdx (dystrophic) and control mice after clenbuterol treatment. (7/192)The mdx mouse is the most commonly used animal model for Duchenne muscular dystrophy. We tested the null hypothesis that 20 weeks of clenbuterol treatment ( approximately 2 mg kg-1 day-1) of mdx and control mice would have no effect on the absolute and specific force (Po, kN m-2) and absolute and normalised power output (W kg-1) of extensor digitorum longus (EDL) and soleus muscles. For mdx and control mice, clenbuterol treatment produced modest increases in the mass of the two muscles but did not increase absolute or specific force or normalised power output. For absolute power output, only the EDL muscles of mdx mice showed a difference following treatment, with the power output of treated mice being 118 % that of the untreated mice. The modest effects of clenbuterol treatment on the dynamic properties of skeletal muscle provide little support for any improvement in muscle function for the dystrophic condition. (+info)
Function and distribution of beta3-adrenoceptors in rat, rabbit and human urinary bladder and external urethral sphincter. (8/192)1. Activation of beta-adrenoceptors causes relaxation of the urinary bladder and contraction of the external urethral sphincter, which consists of fast-contracting skeletal muscles. A beta2-adrenoceptor agonist, clenbuterol, recently has been developed as a therapeutic drug for the treatment of urinary incontinence, however beta2-adrenoceptor agonists have undesirable effects on cardiac and striated muscle function. 2. In this study, we compared the effects of the beta2-adrenoceptor agonist, clenbuterol and of a novel beta3-adrenoceptor agonist, GS332, on urinary bladder and external urethral sphincter function in rat, rabbit and human. We also determined the distribution of beta3-adrenoceptors in human urinary bladder and external urethral sphincter, using radioligand-binding techniques. 3. Clenbuterol induced marked relaxations in rat, rabbit and human urinary bladder smooth muscles and also induced marked contractions in rat periurethral striated muscles (external urethral sphincter), while GS332 induced marked relaxations in rat and human, but not in rabbit, urinary bladder smooth muscles and induced small contractions in rat periurethral striated muscles. 4. The radioligand binding studies showed presence of beta2- and beta3-adrenoceptors in human urinary bladder, external urethral sphincter and abdominal rectus muscles. The affinities of GS332 were the highest in urinary bladder and the lowest in the skeletal (abdominal rectus) muscles, while the affinities of clenbuterol were similar in urinary bladder, external urethral sphincter and the skeletal (abdominal rectus) muscles. 5. These results suggest that GS332 could, similarly clenbuterol, have a role in the treatment of urinary frequency and urinary incontinence. (+info)
β2-Agonist clenbuterol suppresses bacterial phagocytosis of splenic macrophages expressing high levels of macrophage receptor...
TY - JOUR. T1 - β2-Agonist clenbuterol suppresses bacterial phagocytosis of splenic macrophages expressing high levels of macrophage receptor with collagenous structure. AU - Shirato, Ken. AU - Sato, Shogo. AU - Sato, Madoka. AU - Hashizume, Yoko. AU - Tachiyashiki, Kaoru. AU - Imaizumi, Kazuhiko. PY - 2013/3. Y1 - 2013/3. N2 - Splenic marginal zone macrophages expressing macrophage receptor with collagenous structure (MARCO) contribute to the clearance of blood-borne pathogens. We determined a splenic adherent cell fraction abundantly containing cells expressing a higher level of MARCO by flow cytometry, and examined the effects of daily administration of an anabolic dose of β2-agonist clenbuterol on the phagocytic capacity of the cells in mice. After 6 weeks of clenbuterol (1.0 mg/kg body weight/d) or vehicle administration to the mice, splenic adherent cells were isolated. These cells were separated into three cell-size subpopulations. Among them, the small-cell subpopulation contained ...
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Clenbuterol is a beta-2 receptor which works similar to ephedrine or amphetamine in short term. Using Clenbuterol leads to increase in body temperature, heart rate, and blood pressure. Clenbuterol is also called as 5-dichlorobenzyl alcoholic monohydrochloride or Clenbuterol hydrochloride. This guide will brief you more about Clenbuterol and its effects on weight loss.. Medical Advantages Of Clenbuterol. When you take Clenbuterol, it gets absorbed in body and after that, stays in blood system for about 25 to 40 hours. On account of its long life span, it works well in users body for longer time. After taking it, it gets absorbed within 20 minutes. Users liver metabolizes Clenbuterol and it gets excreted from body in the form of urine while about 5 percent gets removed through facial pores in form of sweat.. Health care practitioners usually prescribe Clenbuterol to the people suffering inflammatory diseases and bronchopneumonia. Impact of Clenbuterol depends upon distribution of ...
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Clenbuterol shortly called Clen is used mostly by fitness professionals to enhance performance and to improve their physique. This steroid also known as size zero pill and acts extremely well as a fat burner due to its thermogenic properties. Celebrities use this steroid more as one of the major uses of Clen is to induce weight loss and to maintain a perfect body. However, even many bodybuilders and athletes use this drug because it has an excellent ability to preserve muscle mass. Clenbuterol is available in three types that are either in pill form or liquid form or powder form. However, Powder Clenbuterol is not widely available in steroid market like the liquid and pills forms of this drug. So most people take Clenbuterol either as tablets or as the liquid formulation. Clenbuterol HCL syrup for weight loss is more effective than the Clenbuterol tablets because syrup helps you lose weight more quickly than the tablets.. Clenbuterol in the form of injection might not be the best option even for ...
Beneficial wound healing and metabolic effects of clenbuterol in burned and nonburned rats<...
TY - JOUR. T1 - Beneficial wound healing and metabolic effects of clenbuterol in burned and nonburned rats. AU - Hollyoak, Maureen A.. AU - Muller, Michael J.. AU - Meyers, Nicholas A.. AU - Williams, William G.. AU - Barrow, Robert E.. AU - Herndon, David N.. PY - 1995/1/1. Y1 - 1995/1/1. N2 - Clenbuterol is known to increase muscle mass in nonburned and burn-injured subjects. The effects of clenbuterol on wound healing and the postburn response were examined in both nutritionally matched and free-feeding groups of rats. Rats received either a sham or 30% total body surface area scald burn and then a dorsal incision. Clenbuterol (2 mg/kg/day) was administered subcutaneously via a miniosmotic pump. The burn injury resulted in a sustained non-temperature-dependent hypermetabolism that was not altered by clenbuterol. Clenbuterol induced muscle anabolism and body growth in sham and burned-injured animals. Treated sham animals demonstrated increased wound breaking strength. Matched nutritional ...
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Why Clenbuterol?. There are many supplements out there that help you lose weight and gain muscle, so what is so special about this particular name? First, it works, and not all the products on the market can do this as you desire. The results are fast, long-lasting, and make you feel good about what you are doing. The product is safe and highly-effective and is one of these products that people cannot stop talking about. If you want a product that helps you burn fat and build muscle without any ill side effects, this is the perfect product.. Clenbuterol Facts. A few additional Clenbuterol facts important to know:. - Clenbuterol can be used by men and women. - The product is manufactured in several different dosing forms. - You should start your cycle of Clenbuterol with the lowest dosage amount and increase it as needed. - An allergic reaction to the product is possible. Although Clenbuterol is not approved by the FDA, thousands of people have used the product and benefit greatly. You can be the ...
Muscle protein waste in tumor-bearing rats is effectively antagonized by a beta 2-adrenergic agonist (clenbuterol). Role of the...
Tissue protein hypercatabolism (TPH) is a most important feature in cancer cachexia, particularly with regard to the skeletal muscle. The rat ascites hepatoma Yoshida AH-130 is a very suitable model system for studying the mechanisms involved in the processes that lead to tissue depletion, since it induces in the host a rapid and progressive muscle waste mainly due to TPH (Tessitore, L., G. Bonelli, and F. M. Baccino. 1987. Biochem. J. 241:153-159). Detectable plasma levels of tumor necrosis factor-alpha associated with marked perturbations in the hormonal homeostasis have been shown to concur in forcing metabolism into a catabolic setting (Tessitore, L., P. Costelli, and F. M. Baccino. 1993. Br. J. Cancer. 67:15-23). The present study was directed to investigate if beta 2-adrenergic agonists, which are known to favor skeletal muscle hypertrophy, could effectively antagonize the enhanced muscle protein breakdown in this cancer cachexia model. One such agent, i.e., clenbuterol, indeed largely ...
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Negative effect of clenbuterol on physical capacities and neuromuscular control of muscle atrophy in adult rats. - Etap Lab
INTRODUCTION: Clenbuterol has been used to alleviate chronic obstructive pulmonary disease and elicit an anabolic response in muscles. The aim of this study was to determine the influence of muscle mass variation on physical capacities in rats.. METHODS: The left hindlimbs of Wistar rats were immobilized for 20 days in plantarflexion with a splint and then remobilized for 16 days. The effect of a non-myotoxic dose of clenbuterol during the immobilization period was evaluated. Physical capacities were coordination, free locomotion, grip strength, and bilateral deficit.. RESULTS: Immobilization induced a loss of muscle mass, coordination, and strength without any effect on free locomotion. The positive anabolic effect of clenbuterol did not prevent a loss of physical capacities resulting from immobilization.. CONCLUSIONS: Muscle mass correlated strongly with coordination and isometric strength in untreated rats. Anabolic effect, fiber phenotype modification, and perturbation in neuromuscular ...
Amelioration of denervation-induced atrophy by clenbuterol is associated with increased PKC-alpha activity<...
TY - JOUR. T1 - Amelioration of denervation-induced atrophy by clenbuterol is associated with increased PKC-alpha activity. AU - Sneddon, Alan Arthur. AU - Delday, Margaret Inkster. AU - Maltin, Charlotte. PY - 2000/7. Y1 - 2000/7. N2 - Rat soleus muscle was denervated for 3 or 7 days, and total membrane protein kinase C (PKC) activity and translocation and immunocytochemical localization of PKC isoforms were examined. Dietary administration of clenbuterol concomitant with denervation ameliorated the atrophic response and was associated with increased membrane PKC activity at both 3 (140%) and 7 (190%) days. Of the five PKC isoforms (alpha, epsilon, theta, zeta, and mu) detected in soleus muscle by Western immunoblotting, clenbuterol treatment affected only the PKC-alpha and PKC-theta forms. PKC-alpha was translocated to the membrane fraction upon denervation, and the presence of clenbuterol increased membrane-bound PKC-alpha and active PKC-alpha as assayed by Ser(657) phosphorylation. PKC-theta ...
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Clenbuterol, in short Clen is increasingly becoming popular among people for weight loss. Clenbuterol, a member of the alcohol family, is a decongestant and bronchodilator, initially used for the treatment of breathing disorders. It gained popularity, as a weight loss pill, when celebrities showed dramatic changes in their personalities after the use of Clen.. How does Clen work?. Clenbuterol elevates the BMR (base metabolic rate) by increasing the oxygen supply thereby increasing the internal body temperature. As your temperature rises, the mitochondria burn more calories, which if not burnt would have been converted to fat. It specifically targets only fat cells and leaves muscle tissue. Thereby combined with exercise and optimal diet, Clen has positive effects on your overall health.. Problems arise only if Clen is not used in a cycle or is used carelessly. To read more about the negative effects, please click here.. How to buy Clen legally?. Many websites claim that Clenbuterol is illegal in ...
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Affinity of clenbuterol analogues for ß2-adrenoceptors in bovine skeletal muscle and the effect of these compounds on urinary...
The longissimus dorsi muscles of cattle are highly responsive to the anabolic effects of ß2-adrenoceptor agonists, and in the present study were shown to be ß1- rich and homogeneous source of ß2-adrenoceptors. Structural analogues of the ß2-adrenoceptor agonist clenbuterol were prepared in order to examine the relative importance of the benzylic hydroxyl functionality and the aromatic ring halogen substituents in determining the affinity of phenylethanolamines for ß2-adrenoceptors in bovine muscle. It was calculated that the hydroxyl-hydrogen bonding interaction of these compounds contributes only 1-2 kcal/mol to the total binding energy. The aromatic halosubstituents contributed up to 3 kcal/mol to the total binding energy, and we suggest that the relative importance of the latter functionality has been previously underestimated. There was ß1- poor correlation between the affinity of clenbuterol analogues for binding to ß2-adrenoceptors, and the potency of these compounds in reducing urinary
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Because of the mechanism of action of widening or dilating the smooth muscular tissues of the bronchi inside the lungs, athletes perceive that Clenbuterol will also increase oxygen intake.. That can improve delivery of oxygen and other nutrients through the circulation to muscles and other vital organs.. For bodybuilders, this improved oxygen delivery may increase endurance and stamina of the cardiovascular system, enhancing athletic performance.. Technically speaking, the answer to the question - is Clenbuterol legal - is yes, but that does not mean that its harmless.. A number of bodybuilders and non-athletes also take Clenbuterol for its thermogenic or fat burning effects.. Although Clenbuterol does have a small role in the creation of energy and therefore metabolism, a person would have to take inordinately large amounts of the substance to prove beneficial.. Anyone considering use of legal Clenbuterol for weight loss should be aware that it will not work without a nutritious and balanced ...
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When attempting to create a Clenbuterol T3 Cytomel stack, its important to be aware of the dosages and dosage recommendations provided on bodybuilding websites.. Both Clenbuterol and Cytomel T3 require a prescription.. Dosage recommendations for use of either in medical scenarios is vastly different than those recommended by bodybuilders.. For example, when recommended, dosage for Cytomel (tablet form) for the treatment of mild hypothyroidism may start out at 25 mcg a day. A maintenance dose may range between 25 mcg a day and 75 mcg a day.. Bodybuilders typically start out at 20 to 25 mcg Cytomel a day, gradually increasing up to 80 mcg or 100 mcg a week. Dosages for a Clenbuterol T3 Cytomel stack may be even higher, depending on desired results.. Average recommended dosage of Clenbuterol in the treatment of asthma is approximately 20 mcg a day, but may increase up to 40 depending on situation and treatment goals.. When it comes to Clenbuterol, bodybuilding websites often recommend as much as ...
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